Drugs Flashcards
Semisodium Valproate (Depakote)
Used in mania in Bipolar disporder. Is an anticonvulsant. mood stabilizer, reduces seizures. Dissociates to valproate ion in GI, binds and inhibits GABA transaminase, also may block reuptake. may also work by suppressing repetitive neuronal firing through inhibition of voltage-sensitive sodium channels.
Folate antagonist, teratogenic.inhibits the DHFR protein. This enzyme is used to activate folic acid in the human body before it can enter the folate metabolism cycle.
750mg/day
Lithium
Used in mania of Bipolar. anticonvulsant, mood stabaliser. Blocks NMDA receptors, reducing Ca inflow into post synaptic neurons, reducing excitatory effects of glutamate. 1800mg/day
Lamotrigine/lamictal
Bipolar mania. Anticonvulsant mood stabilizer. Blocks Na and Ca channels. dec glutamate release.
Folic acid/THF
prevent neural tube defects. Folate is needed for production of new cells, DNA RNA synthesis and preventing changes to DNA. Crucial role in the closure of anterior and posterior neuropores. Its better to take naturally occuring folates - folinic acid and THF. to prevent first NTD take 400ug daily in first trimester. To prevent reacurrance 4-5mg perday.
NSAIDs
inhibit COX so inhibit prostaglandin production - anti inflam and antipyretic. Thromboxanes - antiplatlet. Anti inflam reduce pain. Increased risk of MI.
Ibruprofen
weak non selective COX inhibitor. 300 - 400mg 3/4 times daily. max 2.4g daily.
Paracetamol
COX inhibitor in CNS mainly COX 2, no anti inflam effects in peripheral tissues. can cause kidney damage and if take 10 to 15g, can cause hepatotoxicity. 0.5-1g every 4-6 hours, max 4g daily.
opioids co codamol and morphine
bind to opioid receptors, mainly u. inhibit adenylyl cyclase so reduce intracellular cAMP. open K channels causing hyperpolarisation. inhibit Ca opening, reduce neurotransmitter release. Prodrug.
Gabapentin
anticonvulsant used to treat neuropathic pain. Inc GABA synaptic conc, by acting as a calcium channel modifier. 300mg on day 1, twice on day 2, thirce on day 3.
Lidocaine
Local anasthetic. blocks Na, preventing AP.
amoxicillin
antibiotic, B lactam ring.
Thrombolysis/tPA(alteplase)
administered within 4.5 hours of stroke. Inactivates thrombin and ADP. tPA is a protease that cleaves plasminogen to form plasmin, which cleaves fibrin and other coagulants to degrade thrombi.
Anticoagulation long term
Warfarin and Heparin, inhibit function of coagulating factors in clot formation.
antiplatlet long term
aspirin/clopidegrol. Inhibit the function of platelets in clot formation. inhibit generation of thromboxane to have antithrombotic effect. Inhibit ADP receptor on platlets, prevents cross linking.
types of drugs for heamorrhagic stroke
anticonvulsants - reduce seizures. antihypertensive reduce BP. osmotic diuretics dec intercranial pressure.
Benzodiazepines (diazepam) in GAD
anticonvulsant. binds to a subunit on GABA a receptor causing the chanell to open and Cl- to influx hyperpolarising the cell, reducing anxiety. Also inc affinity of the receptor to GABA. shouldnt be used for longer than 2 weeks. GABAA receptors lacking a γ subunit are insensitive to benzodiazepines.
sertraline
SSRi. block seratonin reuptake transporter protein. inc conc in synaptic cleft.
venlafaxine
SNRI. blocks seratonin and noradren reuptake.
pregabalin
anticonvolsant treats neuropathic pain in GAD inc GABA synaptic conc.
methylprednisolone, prednisone.
Anti inflammatory in MS. Corticosteroid. avoid long term use. 1g/day for 3 days. 500mg/day for 5 days. Glucocorticoids bind intracellular receptors that then dimerise, migrate to the nucleus, and interact with DNA to modify gene transcription, inducing synthesis of some proteins and inhibiting synthesis of others.
Glucocorticoids dramatically reduce the manifestations of inflammation, inhibiting both the early and the late manifestations of inflammation. This is due to their profound effects on the concentration, distribution, and function of peripheral leukocytes & lymphocytes and to their suppressive effects on the inflammatory cytokines and chemokines and on other mediators of inflammation.
The anti-inflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins.
IFN-B
prevent relapse in MS. Dec tcell proliferation, activation, migration. Administered by SC injection daily.
Copaxane/glatiramer acetate
binds to MHC2 prevent binding to antigens. competes with MBP for binding to t cell receptor inhibits activation of MBP reactive t cells. SC injection daily.
fingolimod/Gilenya
blocks sphingosine 1-phosphate receptor-1 (s1p receptor) trapping lymphocytes in lymph nodes. tablet 0.5mg
Matalizumab/Tysarbi
monoclonal antibody that binds to a4b1 integrin on WBC. This prevents the binding of a4b2 integrin to VCAM1 selectin preventing WBC migrating across the BBB. SE: progressive multifocal leukoenenceohalopathy as a result of activation of John cunningham virus.
terifluromide/aubagio
immunosuppressants. inhibit mitochondrial enzyme dihydroorotate dehydrogenase (DHODH), dec Tcell function.
BG-12/Dimethyl Fumarate
Activates Nrf-2 transcriptional pathway, reducing inflamation.
Reserpine
evidence for MA hypothesis of depression, irreversible VMAT blocker causing monoamines in presynaptic terminal to be broken down by MAO and COMT which caused depression.
MAO inhibitors
Iproniazid, phenelzine/tranylcypromine irreversible MAO inhibitor. Moclobomide reversible. prevents the breakdown of monoamine neurotransmitter and inc activity. Must go on a reduced tyrosine diet.
Triglyceride antidepressents
Amitriptyline. clomipramine. Block reuptake of seratonin noradrenaline and dopamine.
Venlafaxine. Imipramine
SNRI. blocks seratonin and noradren reuptake.
Sertraline, fluoxetine, paroxetine, citalopram, escitalopram, fluvoxamine
SSRI. block seratonin reuptake
Mirtazapine
a2 adrenergic receptor antagonist. neg feedback loop to inhibit release of noradren is blocked so inc release of noradren and seratonin.
antipsychotics
5-HT2A blockers, down regulate the receptor in chronic depression.
co-beneldopa
short acting, cantral and peripherally acting. MAOa inhibitor contraindicated with the use of levadopa. Levadopa precurser for dopamine, decarboxylated into dopamine after crossing BBB, stimulates dopaminergic receptors.
Benserazide/carbidopa peripherally acting DOPA decarboxylase inhibitor. reduces peripheral side effects. cant cross BBB so doesnt prevent effects of levodopa in the brain.
selegiline
irreversible MAOB inhibitor. increases dopamine in the presynaptic neuron after reuptake. allows more dopamine to be repackaged into vesicles via VMAT for subsequent release.
typical antipsychotic – chlopromazine, Haloperidol
dopamine (reduce pos symptoms) and seratonin (elimination of neg symptoms, SE weight gain) and histamine (sedation) receptor antagonist. a-adrenergic receptor antagonist (lower BP). muscarinic receptor antagonist (anticholinergic SE blurred vision.).
Atypical antipsychotics - risperidone, clozapine, quetiapine, olanzopine
block dopamine D2 receptors in ventral striatum, alleviating positive symproms . Block seratonin 2 receptors in mesocortical tract causes an excess of dopamine eliminate neg symptoms.
side effects of antipsychotics
elevated serum prolactin levels - antagonism of dopamine receptors in tuberoinfundibular pathway.parkinsonian symptoms - antag of dopamine receptors in nigrostriatal pathway. weight gain - antag of hist and seratonin receptors plus effects of leptin. Deterioration in working memory - antag of dopamine in mesocortical pathway. blurred near vision - antag of M1 acetylcholine recept. Sedation - antag H1 and a-adrenergic recpet.
Propofol, ketamine, etomidate. sodium thiopemtal
Induction of GA. rapid onset, GABAa receptor antagonist. rarely maintain as slow recovery time when given by IV. administered via IV. SE: hypotention, resp depression.
iso/sevo/desflurane
maintanence of GA. inhaled volatile agent, likely binds to GABA glutamate NMDA and glycine receptors. Given with NO and O2.
fentanyl/morphine
maintanence GA. analgesic. strong agonist at u opioid receptor. inhibits adenyl cyclase which causes inhibition in the release of nociceptive substances like sub P GABA dopamine. IV.
Atracurium
Maintenence GA. muscle relaxant. Non depolarising neuromuscular blocking agent. Block Ach receptors, spontaneously hydrolysed in plasma by respiratory alkalosis. elimination slowed due to respiratory acidosis.
Pancuronium
maintenance GA. muscle relaxant, long acting non depol neuromusc blocking agent. Block Ach recept. Eliminated via renal excretion and metabolism in the liver. its duration can be extended by compromised kidney or liver function.
Suxmethomium/succinylcholine
maintanence GA. muscle relaxent, depolarising neuromusc blocking agent. mimicks Ach without being broken down by acetylcholinesterase leading to desensitization of the neuromusc junction. broken down by butyrylcholinesterase instead.
neostigmine
Reversal of GA. cholinesterase inhibiting drug, blocks Ach thus inc conc so inc muscle contraction. inc at both nicotinic and muscarinic receptors. Treats myasthenia gravis as well. Muscarinic recepts can lead to side E like bradycardia.
glycopyrrolate
Reversal of GA.muscarinic recept antag. limit parasymp effects caused by neostigmime.
atropine
can cross the BBB unlike glycopyrrolate
Manitol
treats raised intercranial pressure and cerebral oedema. osmotic diuretic. inc solute conc in proximal tubule of kidneys. draws water from body into proximal tubule. also inc plasma osmolality inc flow from tissues into interstitial fluid and plasma, reduced intracranial press.
naltrexone/baclofen
blocks opioid receptors and agonist at GABA. eliminates euphoria makes alcohol less rewarding.
disulfiram
causes sickness when alcohol is ingested
acamprosate
reduces craving for alcohol, doesnt cause sickness
dalfampridine
Potassium channel blocker. Exposed potassium channels, due to demyelination, leak K+ ions. This repolarises cells and makes it difficult to trigger an action potential. By blocking the voltage gated K+ channels conduction blocks in demyelinated axons are relieved.
